eBooks

Can you be gluten intolerant without having celiac disease? Can gluten cause symptoms not related to digestion? A growing body of evidence proves that non-celiac gluten sensitivity (NCGS) is not only real, but possibly a larger problem than celiac disease.

An estimated 20 million Americans have thyroid disorders, but more than half don’t know it. Find out why thyroid problems are so often mis-diagnosed, what really causes them, and how to heal them naturally.

Research suggests that healing your gut may be the single most important thing you can do to improve your health. In this eBook, you’ll learn how to optimize your gut health—and by extension, your overall health—with simple diet and lifestyle changes.

What is a low carb diet, really? When can a low carb diet be beneficial? Should everyone follow a low carb diet? Or, can a low carb diet ruin your health? After reading this eBook, you’ll be able to understand the many factors that play into how a person handles a low carbohydrate diet, and whether or not their health will improve on such a plan.

Are common additives to food and supplements like soy lecithin, carrageenan, xanthum gum, and magnesium stearate harmful–or harmless? Read this eBook to find out which ingredients you should be concerned about, and which are safe.

Is sugar “toxic” in any amount—even in natural sweeteners? Are artificial sweeteners safe? What about stevia and xylitol? Cut through the confusion and hype and find out which sweeteners are safe for you and your family.

The Paleo diet has the potential to dramatically improve your health—but the transition doesn’t always go smoothly. In this eBook, you’ll learn the three biggest obstacles to Paleo success, and how to overcome them.

What do memory loss, depression, anxiety, fatigue, nerve pain, and infertility have in common? They can all be caused by B12 deficiency. Find out why B12 deficiency is more common than most doctors think, how to know if you’re deficient, and what to do about it.

Does eating cholesterol and saturated fat really cause heart disease? Are statin drugs as effective as we’re told? Find out what the latest research says in this eBook, and learn how to prevent and treat heart disease naturally.

Categories

Affiliate Disclosure

This website contains affiliate links, which means Chris may receive a percentage of any product or service you purchase using the links in the articles or advertisements. You will pay the same price for all products and services, and your purchase helps support Chris‘s ongoing research and work. Thanks for your support!

I was wondering if you could outline the parameters for LDL particle number and how they increase the risk. For example, <1000 is wnl for my lab report, what about <1200 or <1500, when do we really get concerned? or is it ideal to have it much less than 1000? thanks, amy

“However in order for the LDL to become denser as it becomes smaller it needs to lose a greater percentage of mass vs volume.”

Sorry, that’s incorrect. I meant to say that while this process does describe a denser lipoprotein it’s moving away from the VLDL side of the spectrum, the opposite of what I thought to be true. This process is basically saying the lipoprotein is changing from VLDL to LDL and becoming problematic at the same time.

Sorry, I’m so turned around right now and probably not making any sense. Hopefully someone can get me going in the right direction.

Really enjoyed your presentation. Can you help clear up some confusion I’m having on lipoprotein sizes?

When it comes to LDL you’ve discussed in previous articles/presentations that it’s important to differentiate between LDL size. You used the analogy that Pattern A is larger and buoyant like beach balls and Pattern B is smaller like bbs. Pattern B was said to be problematic. It’s also been stated that it’s VLDL that is problematic and not LDL. This led me to believe that smaller Pattern B and VLDL were essentially the same thing. This can’t be the case, though, because VLDL is the largest of the lipoproteins and they progressively get smaller all the way to HDL which is the smallest. So looking at a representation of VLDL and LDL I would identify VLDL as Pattern A and LDL as Pattern B which would present contradicting ideas based on the previous statements.

In your summit speech when you were discussing the effect of time, you say the LDL particle gets progressively smaller and denser and this is what’s problematic. However in order for the LDL to become denser as it becomes smaller it needs to lose a greater percentage of mass vs volume.

Is this what happens? Or am I combining two different ideas and one isn’t considered accurate anymore? Or when you say smaller do you mean less mass and I have been incorrectly thinking less volume? I wouldn’t think this to be the case because it still doesn’t resolve the issue of VLDL being the largest lipoprotein and simultaneously problematic because of it’s size. As you can see I’m starting to chase my tail on this and would really appreciate if you could help straighten me out.

My views on the relevance of particle size have changed as new research has been published and I’ve learned more. It turns out that the association between particle size and CVD risk disappears when LDL particle number is taken into account. This suggests that it’s not the size of the particle that’s important, but the number of particles. Other lines of evidence support this, such as the observation that people with familial hypercholesterolemia (which carries a 3x greater risk of CHD) have primarily large, buoyant LDL, and that LDL sizes at either extreme (large or small) have decreased affinity for LDL receptor binding. Since the migration of LDL particles into the endothelium is a gradient-driven process, more LDl particles – whether large or small – will generally mean higher risk of atherosclerosis.

In about 6 weeks I’m going to be releasing a new program called the “high cholesterol action plan” with my updated and expanded views on this subject, as well as a practical, step-by-step guide for what to do (or not do) about high cholesterol.

I heard your talk and was surprised the issue of homocysteine was never discussed as a marker for heart disease. High homocysteine levels often are a result of inadequate levels of vitamin B12, B6 and folate (vitamin B9) or an under active thyroid. This is detailed in the book “The Heart Revolution: The Extraordinary Discovery That Finally Laid the Cholesterol Myth to Rest” by Kilmer McCully, M.D. Dr. McCully shows how homocysteine is a more accurate marker for heart disease than testing cholesterol and that a deficiency in certain B vitamins causes damage to arterial walls and cholesterol responds to this damage. Eating foods high in B vitamins along with supplementation reverses this damage and significantly reduces heart disease risk. On page 23 he summarizes major studies. This passage is copied below. You seem ignorant of this research and don’t offer a simple marker that has been shown to identify heart disease risk, except to be concerned about very high cholesterol levels. As Dr. McCully states: “Eating a cholesterol-rich diet doesn’t cause heart disease, and measuring blood levels of cholesterol fails to predict heart disease in most of those who have it.”

Begin book excerpt:

“• In February 1998 investigators at the Harvard School of Public Health published the results of the Nurses’ Health Study, one of the studies that originally set out to prove that cholesterol was causing heart disease. Instead this study has shown that deficiencies of B vitamins are doing the damage. During a fourteen-year period, 80,000 participants answered questionnaires about their food consumption. The study revealed that those nurses with the lowest consumption of folic acid and B6 had the highest death rates from cardiovascular disease and heart attack. • In April 1998 investigators from England published a study of 21,500 men who were followed for almost nine years. Blood homocysteine levels were higher in men who died of heart disease than in men who did not. The higher the blood homocysteine level, the higher the risk of dying from heart disease. • The Physicians Health Study, completed in 1992, showed that among the 14,000 participants, those with high homocysteine were three times more likely to have a heart attack during a five-year period than persons with normal levels. • In the 1996 Nutrition Canada Study of 5,000 people studied for fourteen years, those with the lowest levels of folic acid in the blood were almost twice as likely to die from heart disease as those with the highest levels. • A study from Norway showed that among 587 patients with proven coronary heart disease, risk of death is directly related to the level of homocysteine in the blood. Cholesterol level, on the other hand, did not predict the risk of death.

• The Hordaland Study of 16,000 residents of Bergen, Norway, showed that homocysteine increases in the presence of other known risk factors for heart disease, including male gender, old age, smoking, high blood pressure, elevated cholesterol level, and lack of exercise. • A multicountry study in 1997 showed that the death rate from coronary heart disease is directly related to blood homocysteine levels. In northern European countries, where heart disease is frequent, people have higher blood levels of homocysteine than in southern European countries, where heart disease is less frequent.

The study in Hordaland, Norway, is especially interesting because a variety of factors associated with heart disease were related to high blood homocysteine. Known risk factors for heart disease–aging, male gender, menopause, lack of vegetables and fruits or vitamin supplements, lack of exercise, high blood pressure, and smoking–cause homocysteine levels to rise. The studies from Canada and the Nurses Health Study show directly that death from heart disease is related to dietary deficiencies of folic acid and vitamin B6. The Physicians Health Study and the British study show that elevated blood homocysteine increases the risk of dying from heart disease. All these studies are powerful evidence supporting the validity of the homocysteine theory of heart disease.

There are, in fact, many cases of heart disease in which cholesterol levels are quite normal. Usually these patients have high homocysteine that is independent of cholesterol; remember J.E. from the first case study. In 1990 a study at the Providence V.A. Medical Center showed that the patients with the most advanced arteriosclerosis typically had normal cholesterol levels, and two-thirds of all these patients had no hypertension, diabetes, or elevated cholesterol at all. Only about 15 percent of cases with severe arteriosclerosis had high cholesterol. Eating a cholesterol-rich diet doesn’t cause heart disease, and measuring blood levels of cholesterol fails to predict heart disease in most of those who have it.”

Homocysteine is indeed associated with heart disease, and I’ve read that book. The problem is that lowering homocysteine levels does not seem to prevent heart disease. This suggests that elevated homocysteine is a marker for an underlying process that is contributing to heart disease, and simply lowering homocysteine itself without addressing that underlying process is not sufficient.

Chris, Any chance you will recap your lecture here on your website? I’d gladly pay for your single lecture, but don’t care to purchase the whole paleo summit. Any plans on re-giving it on your podcast?

Hi Chris, I loved your talk at the Paleo Summit and forwarded the link to my mother who has hypothyroid and high cholesterol. Are there any doctors you could refer someone to in Orange County that have some of this great knowledge about cholesterol?

Chris, I’m newly amazed every time I listen to you. You are a gifted teacher with something very important to teach. I may have to purchase the Paleo Summit package just so I can listen to this some more and I don’t even have cholesterol issues!